Endoplasmic Reticulum Stress and Disease

The paper uses Dynamic Organellar Maps to study protein localization changes in yeast during ER stress, revealing widespread relocalization and new insights into ER stress responses.

This study investigates how autophagy, the unfolded protein response, and the cytoplasmic heat stress response interact in maize under heat stress, revealing differential effects of autophagy loss on these pathways.

This study shows WEE1 inhibitors trigger the integrated stress response via GCN2 activation, leading to translational shutdown, which can be mitigated by low-dose or combination treatments.

This study shows that MANF levels decline with age in mice and that MANF deficiency affects neurobehavioral functions differently in males and females.

This study shows hydroxyurea induces ER stress and cytoplasmic protein aggregation through disulfide stress, leading to ER expansion and HSP accumulation.

This study shows RAF inhibitors activate the integrated stress response via direct GCN2 activation, independent of ERK1/2, leading to ATF4 and CHOP expression.

This study shows Ca2+ induces PDIA6 phase separation, enhancing proinsulin folding and preventing aggregation through recruitment of PDIA3.

This study shows PERK promotes MERCS formation and mitochondrial remodelling during adaptive UPR signalling in myoblasts and C. elegans, enhancing physiological function.

The paper uses pooled overexpression screens to identify PIPPI, a novel microprotein involved in the ER stress response, by screening sORFs for cytoprotective effects against 6-thioguanine.

This study shows that Campylobacter jejuni activates the unfolded protein response (UPR) in human intestinal epithelial cells, which contributes to inflammation and pathogenesis.

The paper identifies oligosaccharyltransferase (OST) subunits as key interactors in ER-associated degradation (ERAD), suggesting a role in late stages of quality control beyond N-glycosylation.

The paper identifies unique and shared transcriptional responses to ER stress in various endocrine cell types using mRNA sequencing.

This study shows that inhibiting the integrated stress response (ISR) reduces macrophage inflammation and migration in a mouse model of type 1 diabetes.

This study shows that FICD deficiency protects mice from heart failure by enhancing BiP-mediated UPRER and ER-phagy under stress.

This study shows Fbxo42 promotes degradation of Ataxin-2 granules, enabling Xbp1 translation and triggering cell death during terminal UPR activation.

This study shows PDK4 links ERUPR and mitoUPR, affecting mitochondrial integrity in aging and neurodegeneration.

This study identifies manganese as an IRE1 activator that suppresses tumor growth by inducing apoptosis through the unfolded protein response pathway.

This paper shows that an eIF2B activator rescues neonatal lethality in a VWM mouse model but leads to age-related motor deficits and myelin loss.

This study identifies branch-specific UPR proteomic targets in BRAF-mutant melanoma using DIA LC-MS, revealing differential XBP1s regulation linked to drug tolerance.

This paper identifies VDAC1 as the target of SW016789, a hypersecretion inducer, and shows it causes distinct transcriptomic changes in beta-cells compared to ER stress.

This study investigates how human coronary artery endothelial cells respond to fever-range hyperthermia, finding that the IRE1-autophagy pathway regulates cell function and integrity.

This study shows that activating IRE1α in the lungs during MRSA infection worsens pneumonia by increasing inflammation and cell death, but blocking IRE1α improves survival and reduces lung damage.

This study shows that KUS121 reduces atherosclerosis by maintaining ATP levels and reducing ER stress in endothelial cells.

This paper shows a CTRB2 deletion variant increases pancreatic cancer risk by causing ER stress and inflammation in mice, using a new genetic model.

This study identifies a nonenzymatic role of IRE1 in cancer cell cycle progression and tumor growth, independent of its kinase-RNase activity.

This study shows TMED9 facilitates the ER-to-Golgi transport of misfolded GPI-anchored proteins via the RESET pathway, with its function regulated by BRD4780.

This study identifies AA263 analogs that enhance ER proteostasis by targeting ER protein disulfide isomerases, correcting protein misfolding in disease models.

The paper identifies NEMF-mediated CAT-tailing as a mechanism that directs substrates through distinct degradation pathways during translocation-associated quality control.

This study shows that disrupting DR5 disulfide bonds activates pro-apoptotic signaling and reveals DR5 disulfide bonding as a sensor and effector of ER stress in cancer cells.